TUBULAR DYSFUNCTION FOLLOWING KIDNEY-TRANSPLANTATION

After transplantation the kidney is subjected to rejection and other d eleterious factors including ischemic damage, acute tubular necrosis, rejection and the use of cyclosporine A (CsA) or FK506. As a result, k idney damage may be generalized with azotemia as its hallmark. These t ubular syndromes may cause profound changes in the acid base balance a nd in the level of certain blood electrolytes and minerals. As a gener al rule, the renal tubular acidosis (RTA) that appears early following transplantation disappears spontaneously and is predominantly a seque la to acute renal failure. On the other hand, defects occurring in the late posttransplant period are often due to chronic rejection or CsA- induced nephrotoxicity. Secondary hyperparathyroidism, urinary tract i nfection and obstructive uropathy may also play a contributory urinary role in the pathogenesis of RTA. Chronic RTA following transplantatio n may interfere with bone metabolism and at times lead to nephrocalcin osis and nephrolithiasis. Therefore, if the condition is prolonged, a supplement of bicarbonate should be given if for no other reason than to protect the skeleton. As these patients may develop either hyperkal emia or hypokalemia, treatment with potassium supplements or potassium -sparing diuretics should be carried out with caution and under consta nt surveillance. Furthermore, magnesium replacement may be advisable i f hypomagnesemia by decreased proximal reabsorption becomes clinically evident. Tubular dysfunction may occur following renal transplantatio n even in patients with maintained glomerular filtration rate and may induce a number of clinical problems including deterioration of renal graft function.